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B Turlin

Publications and source records attributed to B Turlin.

At least 55 records · Page 3Linked to original sources
PubMed1996

[Liver mesenchymal hamartoma in adulthood. Report of a new case].

A case of hepatic mesenchymal hamartoma, found after sudden onset clinical and biological cholestasis, is reported in a 18-year-old man. Abdominal ultrasound examination and computed tomography showed a intrahepatic cystic tumor. The diagnosis of hepatic mesenchymal hamartoma was made by the pathological examination of the resected specimen. This rare tumor is found in most cases in children less than 2 years old. Thirteen cases in adulthood were already reported, five of them in Japanese patients. Our case is peculiar because no hepatic tumor was shown by ultrasound examination, 2 years before, the large size of cysts and presence of smooth muscle fibers in the wall.

Adolescent↗
PubMed1995

Centrilobular necrosis after orthotopic liver transplantation: a longitudinal clinicopathologic study in 71 patients.

Centrilobular necrosis (CLN) is a histological finding often encountered after orthotopic liver transplantation, but its pathogenesis is still unknown. In this study, the significance of CLN was assessed in a series of 227 consecutive liver transplantations performed between January 1989, and December 1991. Seventy-one patients (30.9%) showed CLN on at least one biopsy result, which were obtained because of an increase of aspartate aminotransferase activity. Their liver specimens were reviewed, and 19 histological features were recorded with particular attention given to lobular changes in acinar zone 3, to features commonly attributed to cellular and ductopenic rejection, and to changes suggestive of ischemia. CLN could first be observed either soon (within 4 days) or late (up to 3 years) after transplantation. Only 23 (32.4%) specimens had centrilobular necrosis affecting more than 75% of acinar zones 3. In 60 cases (84.5%) the lesion was limited to acinar zone 3. An important associated feature was sinusoidal congestion in 73.2% of cases. Fifty-one of 71 patients (71.8%) had histological features of cellular rejection before or at the time of CLN, and 13 of these progressed to ductopenic rejection versus 3 of the 156 patients without CLN (P < .0001). Nine patients had a recurrence of CLN, of whom 2 progressed to ductopenic rejection, a recurrence rate of 16.7% in this series. The survival of patients with CLN is worsened by associated ductopenic portal tracts compared with those without ductopenia (P = .0189-Mantel-Cox). This histological combination, irrespective of the serum bilirubin level, may warrant an early conversion to FK506-based immunosuppression.

Adult↗
PubMed1995

Increased liver iron stores in patients with hepatocellular carcinoma developed on a noncirrhotic liver.

Iron was systematically studied in the nontumorous liver of 24 patients with hepatocellular carcinoma (HCC) developed on a noncirrhotic liver compared with 4 control groups (cirrhosis with and without HCC, liver metastasis, and normal liver) matched according to age, sex, and presence of chronic alcoholism. Assessment of liver iron was made by (1) histology according to iron distribution and quantification (total iron score: 0 to 60), and (2) biochemistry (liver iron concentration-N < 36 mumol/g) with calculation of the hepatic iron index (liver iron concentration/age). Patients with hepatocellular carcinoma developed on a noncirrhotic liver presented with (1) histological iron in 83%; (2) parenchymal iron excess significantly more frequent (90%) than in controls; (3) total iron score (15 +/- 12) and liver iron concentration (81 +/- 96) significantly greater than in controls; and (4) hepatic iron index significantly increased (1.4 +/- 1.5) when compared with control groups, except for the hepatocellular carcinoma complicating cirrhosis group (0.9 +/- 1.1). This study (1) shows a mild but unquestionable parenchymal iron excess in the nontumorous liver of most patients presenting with hepatocellular carcinoma developed on a noncirrhotic liver and, at a lesser extent, on cirrhosis, (2) should incite others to study the putative role of iron in the development of liver cancer both in patients with cirrhosis and those without it, whatever the cause of the underlying liver disease, and (3) add argument to take into account and to treat any liver iron excess, even when mild.

Adolescent↗
PubMed1995

[Extrapulmonary mycobacterial infection with multiple cold abscesses].

We report one case of extrapulmonary mycobacterial infection, in the absence of HIV infection, singular by a clinical presentation simulating a tumor, associating a bulky intrahepatic mass, an abscess of the psoas, multiple intracerebral lesions, and an obstructive intracardiac mass of the right ventricle, which required a surgical resection. We comment the type of the mycobacterium involved and the hepatic and cardiac localisations, since macronodular hepatic abscesses are rare, and cardiac abcesses, exceptional.

Adult↗
PubMed1995

Interferon and ursodeoxycholic acid combined therapy in the treatment of chronic viral C hepatitis: results from a controlled randomized trial in 80 patients.

Because 70% to 75% of patients with chronic hepatitis C either do not respond to or relapse after interferon (IFN) therapy, and because ursodeoxycholic acid (UDCA) has been shown to reduce aminotransferase levels in patients with chronic hepatitis, we undertook a prospective controlled randomized trial of IFN (group I) versus IFN plus UDCA (group II) in 80 patients with chronic hepatitis C. IFN was administered in both groups for 6 months (3 to 5 million units [MU] three times a week), and in group II UDCA (10 mg/kg/d) was administered with IFN and then alone for 3 additional months. Response to therapy was defined as the normalization of alanine transaminase (ALT) levels. The results showed that 6 months after cessation of IFN, 59% of responders had relapsed in group I but only 27% had relapsed in group II (P = .03). There was no difference between the two groups for the initial (month 6) and the late (months 15 and 18) response rates to IFN. There was no virological effect or significant histological improvement attributable to the addition of UDCA to IFN treatment. In conclusion, the results of this study show that the addition of UDCA to IFN therapy significantly prolongs the period for which serum ALT remain, within the normal range after discontinuation of IFN. Further studies would be required to determine whether UDCA has any potential for long-term amelioration of the histological severity of liver disease caused by hepatitis C virus (HCV) infection, and, therefore, whether it could be advocated as an adjunct to antiviral therapy.

Adult↗
PubMed1995

[Laryngeal cytomegalovirus infection after heart transplantation].

The authors report a case of laryngeal ulceration due to cytomegalovirus occurring in a 60-year-old man one month after heart transplant. The recipient was initially CMV seronegative and the donor positive. No preventive treatment was administered. One month after the transplantation, search for CMV in blood and urine became positive and a seroconversion occurred. Laryngeal biopsy showed an inflammatory reaction with cells containing atypical inclusions and positivities with anti-CMV antibody. Usual intranuclear eosinophilic inclusions of classic CMV infection were absent. The authors stress the unusual site of the lesions in this primo-infection and the atypical aspect of the inclusions. Such atypical inclusions which have already been reported in immunosuppressed people make the diagnosis more difficult.

Cytomegalovirus Infections↗
PubMed1994

Serum increase and liver overexpression of carbohydrate 19.9 antigen in patients with genetic haemochromatosis.

CA 19.9 antigen is mainly secreted by biliary and pancreatic duct cells. Its metabolism could be modified in genetic haemochromatosis by iron accumulation within these cells. Therefore, CA 19.9 was assayed in the serum samples of 84 patients with genetic haemochromatosis before and after iron depletion and immunolocalised in the liver of 24 untreated genetic haemochromatosis cases. The study showed that serum CA 19.9 (N < 37 IU/l) was increased (SD) before treatment (41.2 (34)) when compared with after the venesection period (16 (12)), and correlated, before treatment, with the amount of iron excess, transaminases, fibrosis, and biliary iron deposits. Hepatic CA 19.9 was located within the cytoplasm of bile duct and cholangiolar cells. In conclusion, this study shows that a mild, reversible, and non-specific increase in serum CA 19.9 is common in genetic haemochromatosis patients and shows that this increase is related to iron excess, directly or through associated liver damage. The unexplained finding of a mild increase in serum CA 19.9 should lead, in a patient with no diagnosis, to the search for liver iron overload, and, in a patient with untreated genetic haemochromatosis, not to further diagnostic procedures unless this finding persists after completion of the venesection treatment.

Alkaline Phosphatase↗
PubMed1993

Primary liver cancer in genetic hemochromatosis: a clinical, pathological, and pathogenetic study of 54 cases.

BACKGROUND: Although liver cancer arises frequently in the course of genetic hemochromatosis (GH), it has not been previously studied in a large series of patients with well-defined GH. METHODS: The bioclinical and pathological data from 1 cholangiocarcinoma and 53 hepatocellular carcinomas (HCCs) complicating GH in 32 untreated and 22 de-ironed patients are reported. RESULTS: This study (1) adds three new well-documented cases of HCC in noncirrhotic but only fibrotic hemochromatotic liver, (2) shows the high prevalence (83%) of proliferative and often dysplastic (70%) iron-free foci in the nontumorous liver of untreated patients, and (3) emphasizes the significant increase of cirrhosis (81% vs. 28%) and of associated noniron-related risk factors, mainly chronic alcoholism (48% vs. 25%) and tobacco smoking (50% vs. 18%) in patients with HCC compared with matched hemochromatotic patients without HCC. CONCLUSIONS: These data (1) suggest that iron-free foci may be markers of an early stage of HCC in GH and (2) supply the basis for defining a cost-effective policy for the screening of HCC in GH patients.

Female↗
PubMed1993

Preneoplastic significance of hepatic iron-free foci in genetic hemochromatosis: a study of 185 patients.

Sublobular nodules of hepatocytes free of iron or exhibiting much less iron than the surrounding parenchyma, referred to in this study as iron-free-foci, are frequently found in the livers of patients with genetic hemochromatosis complicated by hepatocellular carcinoma. To test the hypothesis that such nodules are preneoplastic lesions, iron-free foci were sought in the initial liver biopsy specimens of 185 patients with untreated and uncomplicated genetic hemochromatosis. Iron-free foci were found in 14 (7.6%) patients, all men, aged from 38 to 76 yr, with heavy iron overload and with fibrosis or cirrhosis. Twelve patients with iron-free foci were followed for 0.9 to 15 yr (7 +/- 6 yr). In six (50%), HCC developed, compared with 2 (8%) from a control group consisting of 24 patients without IFF matched according to age, sex, degree of fibrosis, liver iron amount and follow-up duration. The mean number of iron-free foci per iron-free foci-positive specimen was 3.2 +/- 2.1. Ten patients had dysplastic aspects in their iron-free foci, and four had intrahepatocytic iron-positive inclusions at the periphery of iron-free foci. Proliferative cell nuclear antigen was positive in 75% of iron-free foci and in 24% +/- 21% of hepatocyte nuclei in iron-free foci. This study clearly demonstrates that iron-free foci are proliferative lesions and strongly suggests that such nodules are preneoplastic foci. Therefore the finding of IFF in the initial liver biopsy specimen from a patient with genetic hemochromatosis should lead to regular screening for hepatocellular carcinoma.

Adult↗
PubMed1993

Cytokines down-regulate expression of major cytochrome P-450 enzymes in adult human hepatocytes in primary culture.

Cytokines are thought to cause the depression of cytochrome P-450 (CYP)-associated drug metabolism in humans during inflammation and infection. We have examined the role of five cytokines, i.e., interleukin-1 beta, interleukin-4, interleukin-6, tumor necrosis factor-alpha, and interferon-gamma, on the expression of CYP1A2, CYP2C, CYP2E1, CYP3A, and epoxide hydrolase in primary human hepatocyte cultures. Steady state P-450 and epoxide hydrolase mRNA levels, as well as ethoxyresorufin-O-deethylase and nifedipine oxidation activities, which are mainly supported by CYP1A1/1A2 and CYP3A, respectively, were measured. Interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha were found to be the most potent depressors of P-450 enzymes. After 3 days of treatment, both mRNA levels and enzyme activities were depressed, typically by at least 40%, whatever the cytokine and the enzyme considered. Interferon-gamma also suppressed CYP1A2 and CYP2E1 mRNA levels and ethoxyresorufin-O-deethylase activity but had no effect on CYP3A and epoxide hydrolase mRNAs. In addition, interleukin-4 had the opposite effect, compared with other cytokines, on CYP2E1 mRNA, which was increased up to 5-fold; ethoxyresorufin-O-deethylase and nifedipine oxidation activities were not significantly affected. These results provide the first demonstration that various cytokines act directly on human hepatocytes to affect expression of major P-450 genes and that a wide range of responses can be observed among the enzymes for a given cytokine, suggesting that different regulatory mechanisms may be involved.

Adult↗
PubMed1993

[Myxoma of the tricuspid valve. Apropos of a case].

The authors report the case of a chance echocardiographic finding of a tricuspid valve myxoma. Transesophageal echocardiography provided valuable complementary information concerning the precise location of the tumour. Tricuspid valve myxoma is a very rare condition: a review of the literature recensed 16 other cases. This case is of particular interest because of the associated pathological signs: erythemato-papular skin lesions which regresses after ablation of the tumour and a multinodular goitre with a cold isthmic nodule which raised the possibility of the diagnosis of Carney's complex.

Aged↗
PubMed1993

Differentiation between heterozygotes and homozygotes in genetic hemochromatosis by means of a histological hepatic iron index: a study of 192 cases.

The biochemical hepatic iron index, defined as the ratio of hepatic iron concentration (expressed as micromoles per gram dry weight) to age permits accurate prediction of genetic status in patients with genetic hemochromatosis. However, the hepatic iron concentration is not always available. Therefore a histological hepatic iron index, defined as the ratio of total histological iron score (range = 0 to 60) to age, was evaluated in a total of 192 Australian and French patients with genetic hemochromatosis. These subjects had been classified previously as heterozygotes (n = 18) or homozygotes (n = 174) according to clinical and familial data only. Biochemical hepatic iron index and histological hepatic iron index were well correlated (Spearman's test: rho = 0.75, p < 0.0001). Both were significantly (p < 0.0001) increased in homozygotes (respectively, 6.7 +/- 3.8 [range = 1.2 to 22.6] and 0.62 +/- 0.28 [range = 0.14 to 1.5]) compared with heterozygotes (respectively, 1 +/- 0.4 [range = 0.45 to 1.6] and 0.08 +/- 0.05 [range = 0 to 0.14]). The histological hepatic iron index was less than 0.15 in all heterozygotes and greater than 0.15 in all but two homozygotes. These data show that the age-dependent nature of iron accumulation can also be accommodated by calculating the histological hepatic iron index and that histological study is an accurate means of predicting the genetic status of hemochromatosis patients when hepatic iron concentration is not available.

Adult↗
PubMed1992

Liver pathology in genetic hemochromatosis: a review of 135 homozygous cases and their bioclinical correlations.

Liver pathology was assessed in 135 patients with well-defined genetic hemochromatosis ranging from mild disease to severe overload. Three lesions were clearly linked to iron-overload intensity--scarce sidero-necrosis, mild inflammation, and progressive fibrosis. Iron-free foci made of typical or dysplastic hepatocytes were found in 7.4% of the cases. An original grading allowed a reliable quantification of iron and the study of cellular and lobular distribution of iron, which permitted (a) the accurate identification of a decreasing iron gradient in hepatocytes from zone 1 to zone 3 in all cases, (b) the definition of a threshold hepatocytic/mesenchymal iron ratio related to the appearance of sidero-necrosis and to the development of fibrosis, and (c) demonstration that non-iron-related factors (mainly alcoholism) could shift iron from hepatocytes to sinusoidal cells without an increase in the total liver iron amount. This study provides a dynamic view of the iron overload process and suggests that sidero-necrosis and progressive sinusoidal iron overload play a role in the development of fibrosis in human genetic hemochromatosis.

Adolescent↗